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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep-related breathing disorders (SRBDs) represent a spectrum of abnormalities that range from simple snoring to upper airway resistance syndrome to sleep apnea. The clinical presentation may include obesity, snoring, neuropsychological dysfunction, and daytime hypersomnolence and tiredness. The acute hemodynamic alterations of obstructive sleep apnea include systemic and pulmonary hypertension, increased right and left ventricular afterload, and increased cardiac output. Earlier reports attributed the coexistence of SRBDs with cardiovascular diseases to the shared risk factors such as age, sex, and obesity. However, recent epidemiologic data confirm an independent association between SRBDs and the different manifestations of cardiovascular diseases. Possible mechanisms may include a combination of intermittent hypoxia and hypercapnia, repeated arousals, sustained increase in sympathetic tone, reduced baroreflex sensitivity, increased platelet aggregation, and elevated plasma fibrinogen and homocysteine levels. The strength of the association, its pathogenesis, and the impact of treatment of SRBDs on the health outcome of patients with cardiovascular diseases are issues to be addressed in future studies.
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PMID:Cardiovascular consequences of sleep-related breathing disorders. 1235 Feb 42

The contribution of respiratory muscle fatigue to the development of ventilatory failure has been the subject of considerable interest and has stimulated much research. Experimental studies in dogs have shown respiratory muscle fatigue to be a cause of ventilatory failure in both cardiogenic and septic shock models. In clinical conditions resulting in acute or chronic hypercapnia, respiratory muscle fatigue is believed to occur; however, the specific role of fatigue has been difficult to prove.
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PMID:Respiratory muscle fatigue. 1238 Jan 65

Acetazolamide (Acz) is used at altitude to prevent acute mountain sickness, but its effect on exercise capacity under hypoxic conditions is uncertain. Nine healthy men completed this double-blind, randomized, crossover study. All subjects underwent incremental exercise to exhaustion with an inspired O(2) fraction of 0.13, hypoxic ventilatory responses, and hypercapnic ventilatory responses after Acz (500 mg twice daily for 5 doses) and placebo. Maximum power of 203 +/- 38 (SD) W on Acz was less than the placebo value of 225 +/- 40 W (P < 0.01). At peak exercise, arterialized capillary pH was lower and Po(2) higher on Acz (P < 0.01). Ventilation was 118.6 +/- 20.0 l/min at the maximal power on Acz and 102.4 +/- 20.7 l/min at the same power on placebo (P < 0.02), and Borg score for leg fatigue was increased on Acz (P < 0.02), with no difference in Borg score for dyspnea. Hypercapnic ventilatory response on Acz was greater (P < 0.02), whereas hypoxic ventilatory response was unchanged. During hypoxic exercise, Acz reduced exercise capacity associated with increased perception of leg fatigue. Despite increased ventilation, dyspnea was not increased.
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PMID:Acetazolamide reduces exercise capacity and increases leg fatigue under hypoxic conditions. 1239 Oct 68

V(A)/Q mismatching and load/capacity imbalance are the major physiologic determinants of chronic respiratory failure. The former underlies lung failure and the consequent development of hypoxemia. The latter causes chronic ventilatory failure and hypercapnia. This is the consequence of an inefficient breathing pattern with lower VT and higher respiratory rate, probably due to the "wise choice" of preventing excessive inspiratory effort and eventually respiratory muscle fatigue. In many disorders, V(A)/Q mismatching and the load/capacity imbalance coexist, particularly in COPD, where the interplay between the two pathophysiologically represents the advanced stage of the disease. In other disorders, one of the two mechanisms prevails; for example, V(A)/Q mismatching in pure lung diseases, and chest wall mechanics in thoracic disorders. This has important therapeutic implications because oxygen administration can relieve hypoxemia, whereas mechanical ventilation can prevent excessive hypercapnia and respiratory acidosis. Although the role of oxygen therapy is well established, the role of chronic mechanical ventilation is still a matter of debate, particularly in COPD. A major task for future research is to achieve the best possible understanding of the pathophysiologic factors predisposing to chronic ventilatory failure, to prevent the progression of the respiratory diseases to the stage when chronic respiratory failure eventually develops.
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PMID:Physiologic factors predisposing to chronic respiratory failure. 1248 63

Respiratory failure occurs due mainly either to lung failure resulting in hypoxaemia or pump failure resulting in alveolar hypoventilation and hypercapnia. Hypercapnic respiratory failure may be the result of mechanical defects, central nervous system depression, imbalance of energy demands and supplies and/or adaptation of central controllers. Hypercapnic respiratory failure may occur either acutely, insidiously or acutely upon chronic carbon dioxide retention. In all these conditions, pathophysiologically, the common denominator is reduced alveolar ventilation for a given carbon dioxide production. Acute hypercapnic respiratory failure is usually caused by defects in the central nervous system, impairment of neuromuscular transmission, mechanical defect of the ribcage and fatigue of the respiratory muscles. The pathophysiological mechanisms responsible for chronic carbon dioxide retention are not yet clear. The most attractive hypothesis for this disorder is the theory of "natural wisdom". Patients facing a load have two options, either to push hard in order to maintain normal arterial carbon dioxide and oxygen tensions at the cost of eventually becoming fatigued and exhausted or to breathe at a lower minute ventilation, avoiding dyspnoea, fatigue and exhaustion but at the expense of reduced alveolar ventilation. Based on most recent work, the favoured hypothesis is that a threshold inspiratory load may exist, which, when exceeded, results in injury to the muscles and, consequently, an adaptive response is elicited to prevent and/or reduce this damage. This consists of cytokine production, which, in turn, modulates the respiratory controllers, either directly through the blood or probably the small afferents or via the hypothalamic-pituitary-adrenal axis. Modulation of the pattern of breathing, however, ultimately results in alveolar hypoventilation and carbon dioxide retention.
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PMID:Respiratory failure. 1462 Nov 12

Respiratory failure is still an important complication of chronic obstructive pulmonary disease (COPD) and hospitalisation with an acute episode being a poor prognostic marker. However, other comorbid conditions, especially cardiovascular disease, are equally powerful predictors of mortality. The physiological basis of acute respiratory failure in COPD is now clear. Significant ventilation/perfusion mismatching with a relative increase in the physiological dead space leads to hypercapnia and hence acidosis. This is largely the result of a shift to a rapid shallow breathing pattern and a rise in the dead space/tidal volume ratio of each breath. This breathing pattern results from adaptive physiological responses which lessen the risk of respiratory muscle fatigue and minimise breathlessness. Treatment is directed at reducing the mechanical load applied to each breath, correcting specific precipitating factors, e.g. bacterial infection, and maintaining gas exchange. Both bronchodilators and oral corticosteroids can improve spirometric results in exacerbations of COPD and should be routinely offered to patients with respiratory failure. Controlled oxygen is still not always prescribed appropriately and high inspired oxygen concentrations can lead to severe acidosis by either worsening ventilation/perfusion mismatching and/or inducing a degree of hypoventilation. Ventilatory support using noninvasive ventilation has revolutionised the approach to these patients. Acute respiratory failure due to chronic obstructive pulmonary disease remains a common medical emergency that can be effectively managed. More attention should be focused on the prevention of these episodes and identifying the factors which cause early relapse.
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PMID:Respiratory failure in chronic obstructive pulmonary disease. 1462 Nov 14

Noninvasive positive-pressure ventilation (NPPV) should be considered a standard of care to treat COPD exacerbations in selected patients, because NPPV markedly reduces the need for intubation and improves outcomes, including lowering complication and mortality rates and shortening hospital stay. Weaker evidence indicates that NPPV is beneficial for COPD patients suffering respiratory failure precipitated by superimposed pneumonia or postoperative complications, to allow earlier extubation, to avoid re-intubation in patients who fail extubation, or to assist do-not-intubate patients. NPPV patient-selection guidelines help to identify patients who need ventilatory assistance and exclude patients who are too ill to safely use NPPV. Predictors of success with NPPV for COPD exacerbations have been identified and include patient cooperativeness, ability to protect the airway, acuteness of illness not too severe, and a good initial response (within first 1-2 h of NPPV). In applying NPPV, the clinician must pay attention to patient comfort, mask fit and air leak, patient-ventilator synchrony, sternocleidomastoid muscle activity, vital signs, hours of NPPV use, problems with patient adaptation to NPPV (eg, nasal congestion, dryness, gastric insufflation, conjunctival irritation, inability to sleep), symptoms (eg, dyspnea, fatigue, morning headache, hypersomnolence), and gas exchange while awake and asleep. For severe stable COPD, preliminary evidence suggests that NPPV might improve daytime and nocturnal gas exchange, increase sleep duration, improve quality of life, and possibly reduce the need for hospitalization, but further study is needed. There is consensus, but without strong supportive evidence, that COPD patients who have substantial daytime hypercapnia and superimposed nocturnal hypoventilation are the most likely to benefit from NPPV. Adherence to NPPV is problematic among patients with severe stable COPD.
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PMID:Noninvasive ventilation for chronic obstructive pulmonary disease. 1473 24

Despite enormous rates of minute ventilation (Ve) in the galloping Thoroughbred (TB) horse, the energetic demands of exercise conspire to raise arterial Pco(2) (i.e., induce hypercapnia). If locomotory-respiratory coupling (LRC) is an obligatory facilitator of high Ve in the horse such as those found during galloping (Bramble and Carrier. Science 219: 251-256, 1983), Ve should drop precipitously when LRC ceases at the galloptrot transition, thus exacerbating the hypercapnia. TB horses (n = 5) were run to volitional fatigue on a motor-driven treadmill (1 m/s increments; 14-15 m/s) to study the dynamic control of breath-by-breath Ve, O(2) uptake, and CO(2) output at the transition from maximal exercise to active recovery (i.e., trotting at 3 m/s for 800 m). At the transition from the gallop to the trot, Ve did not drop instantaneously. Rather, Ve remained at the peak exercising levels (1,391 +/- 88 l/min) for approximately 13 s via the combination of an increased tidal volume (12.6 +/- 1.2 liters at gallop; 13.9 +/- 1.6 liters over 13 s of trotting recovery; P < 0.05) and a reduced breathing frequency [113.8 +/- 5.2 breaths/min (at gallop); 97.7 +/- 5.9 breaths/min over 13 s of trotting recovery (P < 0.05)]. Subsequently, Ve declined in a biphasic fashion with a slower mean response time (85.4 +/- 9.0 s) than that of the monoexponential decline of CO(2) output (39.9 +/- 4.7 s; P < 0.05), which rapidly reversed the postexercise arterial hypercapnia (arterial Pco(2) at gallop: 52.8 +/- 3.2 Torr; at 2 min of recovery: 25.0 +/- 1.4 Torr; P < 0.05). We conclude that LRC is not a prerequisite for achievement of Ve commensurate with maximal exercise or the pronounced hyperventilation during recovery.
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PMID:Ventilatory dynamics and control of blood gases after maximal exercise in the Thoroughbred horse. 1476 83

Lung hyperinflation is a consequence of airway obstruction, increased airway resistance and compliance in patients with chronic obstructive pulmonary disease (COPD) which may result in respiratory muscle fatigue and deterioration of gas transfer. The aim of this study was to investigate the influence of hyperinflation on respiratory muscles, gas transfer and breathing pattern and compare the differences between mild and severe COPD. Twenty-eight COPD patients with radiological and tomographic evidence of emphysema were included in the study and they were divided into two groups according to the severity of COPD. Group I= FEV(1) < or = 49% (n= 16). Group II= FEV(1) > or = 50% (n= 12). Airflow rates were decreased and airway resistance was increased significantly in Group I. Maximal inspiratory pressure (MIP) was significantly reduced in Group I. FRC, RV and RV/TLC ratio were increased above 120% in both groups with more significant increase in Group I. Group I showed moderate hypoxemia (PaO(2) = 54.02 mmHg) with hypercapnia (PaCO(2)= 46.65 mmHg) whereas Group II patients were mildly hypoxemic (PaO(2)= 63.78 mmHg) with normocapnia. Parameters of breathing pattern were similar in both groups. Diaphragm height index (DHI) didn't showed significant difference between groups. But there were significant correlations between DHI and RV, FRC. MIP showed significant positive correlation with airflow rates and DLCO, negative correlation with lung volumes, positive correlation with PaO(2) and negative correlation with PaCO(2). FRC also negatively correlated with Ti and Ti/Ttot. In conclusion, hyperinflation present even in the mild forms of COPD causes inspiratory muscle weakness which in return results in impairment in gas transfer.
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PMID:[The effect of hyperinflation on respiratory muscles and breathing pattern in COPD]. 1514 1

The effects of hypoxia and hypercapnia on contractile and histological properties of the diaphragm and skeletal muscles of the hind limb were examined. Eight-week-old male Sprague-Dawley rats ( [Formula: see text] ) were kept in hypobaric hypoxic ( [Formula: see text] ) or hypercapnic ( [Formula: see text] ) chambers for 6 weeks, and compared with the control rats (room air, [Formula: see text] ). Contractile properties were evaluated with twitch kinetics, force-frequency curve and fatigue tolerance. After the experiments on contractile activities, muscles were fixed for histological examination with ATPase staining. It was demonstrated that peak twitch tension of diaphragm decreased with no significant histological changes under hypoxic conditions while significant contractile and histological changes were observed under hypercapnic conditions. Skeletal muscles of the hind limbs were affected also under hypoxic and hypercapnic conditions but the profiles of the changes in contraction and histology were different from those of the diaphragm. These results suggest that hypoxia and hypercapnia affect differently on contractile and histological properties of respiratory and hind limb muscles. Furthermore, when we consider the conditions involved in chronic obstructive respiratory disease (COPD; both hypoxia and hypercapnia are deeply involved), our results indicate that COPD should be regarded as a systemic disorder rather than a respiratory disease.
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PMID:Hypoxia and hypercapnia affect contractile and histological properties of rat diaphragm and hind limb muscles. 1517 12


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